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预先诱导的念珠菌特异性全身细胞介导免疫对实验性阴道念珠菌病的影响。

Effects of preinduced Candida-specific systemic cell-mediated immunity on experimental vaginal candidiasis.

作者信息

Fidel P L, Lynch M E, Sobel J D

机构信息

Division of Infectious Diseases, Wayne State University School of Medicine, Detroit, Michigan 48201.

出版信息

Infect Immun. 1994 Mar;62(3):1032-8. doi: 10.1128/iai.62.3.1032-1038.1994.

Abstract

It has been postulated that systemic cell-mediated immunity (CMI) is an important host defense factor against recurrent vaginal infections caused by Candida albicans. Using an estrogen-dependent murine model of vaginal candidiasis, we have previously shown that mice inoculated vaginally with C. albicans acquire a persistent vaginal infection and develop Candida-specific Th1-type systemic CMI. In the present study, experimental vaginitis was monitored in the presence of preinduced systemic Candida-specific CMI. Mice immunized systemically with C. albicans culture filtrate antigens (CaCF) in complete Freund's adjuvant (CFA) had Th1-type reactivity similar to that of vaginally infected mice. CaCF given to mice intravenously induced Candida-specific suppressor T (Ts) cells. Mice preimmunized with CaCF-CFA and given a vaginal inoculum of C. albicans had positive delayed-type hypersensitivity (DTH) reactivity from the time of vaginal inoculation through 4 weeks. Conversely, mice infected in the presence of Ts cells had significantly reduced DTH responses throughout the 4-week period in comparison with naive infected mice. However, the presence of Th1-type Candida-specific DTH cells or Ts cells, either induced in mice prior to vaginal inoculation or adoptively transferred at the time of inoculation, had no effect on the vaginal Candida burden through 4 weeks of infection. A similar lack of effects was obtained in animals with lower Candida population levels resulting from a reduction in or absence of exogenous estrogen. These results suggest that systemic Th1-type CMI demonstrable with CaCF is unrelated to protective events at the level of the vaginal mucosa.

摘要

据推测,全身性细胞介导免疫(CMI)是抵御白色念珠菌引起的复发性阴道感染的重要宿主防御因子。我们先前利用雌激素依赖的小鼠阴道念珠菌病模型表明,经阴道接种白色念珠菌的小鼠会发生持续性阴道感染,并产生念珠菌特异性Th1型全身性CMI。在本研究中,在预先诱导的全身性念珠菌特异性CMI存在的情况下监测实验性阴道炎。用白色念珠菌培养滤液抗原(CaCF)在完全弗氏佐剂(CFA)中进行全身免疫的小鼠具有与经阴道感染小鼠相似的Th1型反应性。给小鼠静脉注射CaCF可诱导念珠菌特异性抑制性T(Ts)细胞。用CaCF-CFA预先免疫并经阴道接种白色念珠菌的小鼠从阴道接种时起至4周内均具有阳性迟发型超敏反应(DTH)反应。相反,与未感染的对照小鼠相比,在Ts细胞存在下感染的小鼠在整个4周期间的DTH反应明显降低。然而,在阴道接种前在小鼠中诱导或在接种时过继转移的Th1型念珠菌特异性DTH细胞或Ts细胞的存在,在感染4周内对阴道念珠菌负荷没有影响。在因外源性雌激素减少或缺乏而导致念珠菌数量水平较低的动物中也得到了类似的无影响结果。这些结果表明,用CaCF证明的全身性Th1型CMI与阴道黏膜水平的保护事件无关。

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